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- ArticleAçık Erişim2021Effect of Rutin on Gentamicin-Induced Ototoxicity in Rats: A Biochemical and Histopathological Examination
Salcan, Ismail; Dilber, Muhammet; Bayram, Rana; Süleyman, Esma; Yazici, Gulce Naz; Çoban, Abdulkadir; Süleyman, Halis
Objective: Gentamicin is a broad-spectrum aminoglycoside antibiotic administered parenterally for moderate to severe gram-negative infections. Ototoxicity is an important side effect that limits gentamicin use. The aim of this study is to investigate the effect of rutin on gentamicin-induced ototoxicity in rats biochemically and histopathologically. Methods: Distilled water was administered by oral gavage to healthy controls (HG) and cobalt administered group (GC). 50 mg/kg rutin was administered by oral gavage to rutin + gentamicin (RGG) group. After one hour, 100 mg/kg gentamicin was injected intraperitoneally (i.p) to the RGG and GC animal groups. This procedure was repeated once a day for 14 days. Results: Malondialdehyde (MDA), nuclear factor-kappa B(NF-kappa B), tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta(IL-1 beta) levels in the cochlear nerve tissue of gentamicin-treated animals were significantly higher compared to healthy controls and rutin + gentamicin treated rats. On the other hand, the amount of total Glutathione (tGSH) was significantly lower compared to the control and rutin group. Histopathological examination revealed degenerated myelinated nerve fibers in the gentamicin group and Schwann cell nuclei were generally not seen. There was a high accumulation of collagen fiber in the tissue and dilated blood capillaries. In the rutin group, myelinated nerve fibers mostly exhibited normal morphology, Schwann cell nuclei were evident and the vessels were normal. Conclusion: Our experimental results suggest that rutin may be effective in the treatment of gentamicin-associated ototoxicity.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Protection against experimental cisplatin-induced optic nerve toxicity using resveratrol: A rat model study
Agcayazi, Sümeyye Burcu; Ugurlu, Adem; Ucak, Turgay; Tasli, Nurdan Gamze; Karakurt, Yucel; Icel, Erel; Keskin Cimen, Ferda; Süleyman, Halis
Aim: To investigate the effects of resveratrol on oxidative stress and inflammation parameters and histological alterations in cisplatin-induced optic nerve damage in a mouse model. Material and Method: Thirty-six albino Wistar male rats were divided into three groups as control, 5 mg/kg cisplatin-administered (Cis) and 5 mg/kg cisplatin + 25 mg/kg resveratrol-administered (Cis + Res) animals. At the end of the experimental period, the rats were sacrificed with high-dose (50 mg/kg) thiopental sodium, and their optic nerves were dissected. Malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS), total antioxidant status (TAS), tumour necrosis factor alpha (TNF-α), nuclear factor kappa B (NF-KB) levels, and histopathological findings were assessed using the optic nerve tissues. Results: In the Cis + Res group, the MDA, TOS, OSI, TNF-a and NFK-B levels were significantly lower and the tGSH and TAS levels were significantly higher compared with the Cis group (P = 0.001). In histological evaluations, there were dilated and congested blood vessels, destruction, oedema, degeneration, haemorrhage, and proliferating capillaries indicating the presence of inflammation and damage only in the Cis-administered group. However, in the Cis + Res group, the histological findings were very similar to the healthy controls. Conclusion: Resveratrol is a promising neuroprotective agent for cisplatin-induced optic nerve toxicity with its anti-oxidant and anti-inflammatory effects. Further investigations are needed to evaluate the possible therapeutic effects on other optic nerve toxicities.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Coenzyme Q10 effect on cisplatin-induced oxidative retinal injury in rats
Sunar, Mukadder; Yazici, Gulce Naz; Mammadov, Renad; Kurt, Nezahat; Arslan, Yusuf Kemal; Süleyman, Halis
Aim: In this study, it was aimed to investigate the effect of coenzyme Q10 (CoQ10) on cisplatin-induced oxidative retinal damage in rats biochemically and histopathologically. Materials and methods: Thirty male Wistar albino rats were divided into 3 groups randomly: untreated control (C group), only 2.5 mg/kg cisplatin daily administrated group for 2 weeks (CP group), 2.5 mg/kg cisplatin + 20 mg/kg orally CoQ10 daily administrated group for 2 weeks (CoQC group). At the end of experimental period, blood samples obtained before sacrification for the biochemical examination of serum malondialdehyde (MDA), total glutathione (tGSH), total oxidant system (TOS), total antioxidant systemic (TAS) levels and after eyes were removed for examined histopathology. Results: As a result of our study, severe histopathological damage was detected in the retinal tissue of the cisplatin group with serum malondialdehyde (MDA) and total oxidant system (TOS) levels were high and total glutathione (tGSH) and total antioxidant systemic (TAS) levels were low. However, it was observed that the histopathological damage associated with cisplatin was decreased in the retinal tissue of the CoQ10 group, which inhibited the increase in blood serum MDA/TOS levels and decrease in tGSH/TAS levels. Conclusion: The biochemical and histopathological results of our study were compatible with each other, so we concluded that the damage to the rat retinal tissue caused by cisplatin may be reversible with coenzyme.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2019The effects of lycopene on alloxan induced diabetic optic neuropathy
Icel, Erel; Icel, Aykut; Uçak, Turgay; Karakurt, Yücel; Elpeze, Burcu; Keskin Çimen, Ferda; Süleyman, Halis
Aim: To determine the effects of lycopene treatment in prevention of diabetes associated inflammatory response and oxidative stress in an experimental model. With this aim we investigated the levels of oxidative stress markers including Malondialdehyde (MDA), and total oxidative status (TOS)together with inflammatory markers including nuclear factor- kappa B (NFKB) and tumor necrosis factor α (TNF-α) and antioxidants including total glutathione (TGSH), total oxidative status (TOS) and total anti-oxidative status (TAS) levels on eye tissue. Material and methods: Totally 18 albino Wistar male rats (250–280 grams) assigned into three groups, with six rats in each group as follows: healthy group (HG), control group (CG), and lycopene group (LG). The diabetes was induced with alloxan administration in rats of CG and LG. Lycopene (4 mg/kg) was administered to the rats in LG once a day for 3 months. At the end of this period, the animals were sacrificed and their eyes were enucleated for histopathological evaluations. From the tissues, MDA, GSH, TOS, TAS, TNF-α and NF-κB levels were analyzed. Results: MDA, TOS, OSI, NFKB and TNF-α levels were significantly higher, while TGSH and TAS levels were significantly lower in CG compared with HG (p < 0.001). On the other hand in LG; MDA, TOS, OSI, NFKB and TNF-α levels were significantly lower, while TGSH and TAS levels were significantly higher compared with CG (p < 0.001). Regarding histopathological findings, although there was severe damage on optic nerve of rats in CG; there was only a slight damage in lycopene administered group. Conclusion: For the first time in literature we determined that, lycopene was significantly effective in prevention of augmented inflammation and oxidative stress on eye tissue associated with diabetes, as well as the tissue damage on optic nerve. However, studies investigating the long-term clinical effects of lycopene on diabetic individuals are warranted.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2019The effect of Hippophae rhamnoides extract on ischemia reperfusion-induced brain injury in rats
Ozbek Bilgin, Asli; Altuner, Durdu; Cankaya, Murat; Cakir, Tayfun; Mammadov, Renad; Bilgin, Yasin; Süleyman, Halis
The aim of this study was to examine the effects of Hippophae rhamnoides extract (HRE), known to have antioxidant properties, on ischemia reperfusion-induced brain injury in rats. Eighteen albino Wistar male rats were divided into three equal groups: 15 min of brain ischemia-3 h of reperfusion (BIR) group, 50 mg/kg HRE + brain ischemia-reperfusion (HRE + BIR) group, and control group for sham operation (SHAM). Malondialdehyde (MDA) level, myeloperoxidase (MPO) activity and 8-OHdG levels significantly increased, whereas total glutathione (tGSH) level, glutathione reductase (GSHRd), glutathione s-transferase (GST) activities decreased in the brain tissues of BIR group compared to SHAM group. HR application reversed these changes and brought the levels closer to the level of SHAM group. This study has revealed that HR inhibits IR-induced oxidative damage and inflammation in rat’s brain biochemically and it is effective in maintaining antioxidant activity and protecting against DNA damage in the tissue.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2019The effects of thiamine pyrophosphate on ethanol induced optic nerve damage
Ucak, Turgay; Karakurt, Yucel; Tasli, Gamze; Cimen, Ferda Keskin; Icel, Erel; Kurt, Nezahat; Ahiskali, Ibrahim; Süleyman, Halis
Background: We aimed to determine the protective effects of thiamine pyrophosphate on ethanol induced optic neuropathy in an experimental model. Methods: The rats were assigned into 4 groups, with 6 rats in each group as follows: healthy controls (HC group), only ethanol administered group (EtOH group), ethanol + thiamine pyrophosphate (20 mg/kg) administered group (TEt-20 group), and only thiamine pyrophosphate (20 mg/kg) (TPG group) administered group. To the rats in TEt-20 and TPG groups, 20 mg/kg thiamine pyrophosphate was administered via intraperitoneal route. To the rats in HC and EtOH groups, the same volume (0.5 ml) of distilled water as solvent was applied in the same manner. To the rats in TEt-20 and EtOH groups, one hour after application of thiamine pyrophosphate or distilled water, 32% ethanol with a dose of 5 g/kg was administered via oral gavage. This procedure was repeated once a day for 6 weeks. From the blood samples and tissues obtained from the rats, Malondialdehyde (MDA), reduced glutathione (GSH), interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) levels were studied. Histopathological evaluations were performed to the optic nerve tissue. Results: Serum and tissue IL-1β, TNF-α and MDA levels were the highest in EtOH group which were significantly lower in thiamine pyrophosphate administered group (TEt-20 group) (p: 0.001). Serum and tissue reduced GSH levels were the lowest in EtOH group which were also significantly higher in TEt-20 group (p:0.001). In histopathological evaluations, in EtOH group there was obvious destruction and edema with hemorrhage and dilated blood vessels which were not present in any other groups. Conclusions: There was an apparent destruction in ethanol administered group in histopathological analyses with an augmented level of oxidative stress markers and all those alterations were prevented with concomitant thiamine pyrophosphate administration. These protective effects of thiamine pyrophosphate are extremely important in chronic ethanol consumption. Clinical studies are warranted to define the exact role of thiamine pyrophosphate in prevention of ethanol induced optic neuropathy.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2019The effects of lutein on optic nerve injury induced by ethambutol and isoniazid: an experimental study
Karakurt, Yucel; Süleyman, Halis; Keskin Cimen, Ferda; Tasli, Gamze; Ucak, Turgay; Icel, Erel; Kurt, Nezahat
Aim: Ethambutol and isoniazid are two major effective first line agents in tuberculosis treatment having some visual adverse effects. We aimed to determine the protective effects of lutein on oxidative optic neuropathy induced by ethambutol and isoniazid in an experimental model. Material and method: Totally 24 albino Wistar male rats were assigned into 4 groups, with 6 rats in each group as follows: healthy controls (HC group), 50 mg/kg ethambutol +50 mg/kg isoniazid administered group (EI), 0.5 mg/kg lutein +50 mg/kg ethambutol +50 mg/kg isoniazid administered group (LEI-05) and only Lutein (0.5 mg/kg) (LUT group) administered group. From the blood samples and tissues obtained from the rats, Malondialdehyde (MDA), total glutathione (GSH), interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) levels were studied. Histopathological evaluations were performed at the end of the study. Results: Serum and tissue IL-1β, TNF-α and MDA levels were the highest in EI group which were significantly lower in lutein administered group. On the other hand, serum and tissue total GSH levels were the lowest in EI group which were significantly higher in Lutein administered group. In histopathological evaluations, there were significant differences between EI group and all other three groups with edema and hemorrhage in connective tissue covering optic nerve, dilated and congested capillary, decrease in astrocytes and oligodendrocytes. Conclusion: Isoniazid and ethambutol induced toxic optic neuropathy although not common, may have some potential devastating effects on vision. Lutein is determined as an effective agent in prevention of isoniazid and ethambutol induced toxic optic neuropathy.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2018Effects of Pycnogenol on cisplatin-induced optic nerve injury: an experimental study
Icel, Erel; Uçak, Turgay; Agcayazi, Burcu; Karakurt, Yücel; Yilmaz, Hayati; Keskin Çimen, Ferda; Süleyman, Halis
Aim: To determine the effects of Pycnogenol on cisplatin-induced optic nerve damage. Material and method: Totally 18 albino Wistar male rats were assigned into three groups, with six rats in each group as follows: healthy controls (HC group), only cisplatin (2.5 mg/kg) administered group (CIS group) and Pycnogenol (40 mg/kg) + cisplatin (2.5 mg/kg) administered group (PYC group). We analyzed the levels of malondialdehyde (MDA) as a marker of lipid peroxidation and oxidative stress, total glutathione (tGSH) as a marker of antioxidant status, nuclear factor-kappa B (NF-κB) and tumor necrosis factor alpha (TNF-α) as inflammatory markers, total oxidative status (TOS) and total antioxidant status (TAS) on eye tissue together with histopathological evaluation of optic nerve in an experimental model. Results: In CIS group MDA, TOS, TNF-α and NF-κB levels were statistically significantly higher (p < 0.001) than HC group while tGSH and TAS levels were significantly lower (p < 0.001). On the other hand, in PYC group MDA, TOS, TNF-α and NF-κB levels were statistically significantly lower (p < 0.001) than CIS group while tGSH and TAS levels were significantly higher (p < 0.001). Conclusion: Pycnogenol pretreatment was highly effective in preventing augmentation of cisplatin-induced oxidative stress and inflammation in eye tissue.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2018The effects of rutin on cisplatin induced oxidative retinal and optic nerve injury: an experimental study
Taşlı, Nurdan Gamze; Uçak, Turgay; Karakurt, Yücel; Keskin Çimen, Ferda; Özbek Bilgin, Aslı; Kurt, Nezahat; Süleyman, Halis
Aim: To determine the role of rutin in prevention of cisplatin induced retinal and optic nerve injury in an experimental study. Materials and methods: Totally 18 albino Wistar male rats were assigned into three groups, as follows: healthy controls (HC group), only cisplatin administered group for 14 days (CIS group), and rutin + cisplatin administered group for 14 days (RC group). Blood samples were obtained from animals just before the scarification. Serum malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH), superoxide dismutase (SOD), interleukin 1 beta (IL-1β) and tumour necrosis factor alpha (TNF-α) levels were investigated. The eyes were enucleated for histopathological evaluations of retina and optic nerve. Results: MDA, MPO, IL-1β and TNF-α levels were statistically significantly higher (p < 0.001) in CIS group compared with other two groups while tGSH and SOD levels were statistically significantly lower (p < 0.001). Regarding these parameters, in CIS group MDA, MPO, IL1β and TNF-α levels were statistically significantly increased with cisplatin administration and giving rutin concomitantly with cisplatin prevented this increase. On the other hand, tGSH and SOD levels were statistically significantly decreased with cisplatin administration and giving rutin concomitantly with cisplatin prevented this decrease. In qualitative analyses of histopathological findings of retina and optic nerve; the results of RC group were similar with the results of healthy controls; but there was statistically significant differences between CIS group and other two groups (p < 0.001). Conclusions: Concomitant rutin administration may prevent the detrimental effects of cisplatin on lipid peroxidation, oxidative stress and inflammation markers and may also avert the histopathological damage on retina and optic nerve. Further studies are warranted to determine the effects of cisplatin and rutin on eye.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2018The effects of lutein on cisplatin-induced retinal injury: an experimental study
Karakurt, Yücel; Uçak, Turgay; Tasli, NurdanGamze; Ahiskali, Ibrahim; Şipal, Sare; Kurt, Nezahat; Süleyman, Halis
Aim: Lutein is one of the most common carotenoids defined in human plasma as having potent anti-oxidant effects. We aimed to determine the biochemical and histopathological effects of lutein on cisplatin-induced oxidative retinal injury in rats. Materials and methods: Twenty-four rats were equally divided into four groups as healthy controls (HC group), only cisplatin (5 mg/kg) administered group (CIS group), Lutein (0.5 mg/kg) + cisplatin (5 mg/kg) administered group (LC group), and only Lutein (0.5 mg/kg) (LUT group) administered group. From the blood samples obtained, serum malondialdehyde (MDA), total glutathione (tGSH), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) levels were investigated. In histopathological analyses, the total retinal thickness, retinal pigment epithelium (RPE), photoreceptor layer (PL), outer nuclear layer (ONL), outer plexiform layer (OPL), inner nuclear layer (INL), inner plexiform layer (IPL), and ganglion cell layer (GCL) were evaluated. Results: MDA, IL-1β, and TNF-a levels were statistically significantly higher (p < 0.001) in CIS group compared with other three groups while tGSH levels were statistically significantly lower (p < 0.001). In subgroup analyses, there was no any statistically significant difference regarding all four parameters analyzed between HC, LC, and LUT groups. In histopathological analyses, cisplatin-induced retinal damage included atrophy and disorganization on outer segment, degeneration and detachment of RPE and PL from choroid, degeneration and edema of INL and IPL, total degeneration of GCL; while cisplatin-induced retinal damage was determined to be significantly prevented with 0.5 mg lutein treatment on histopathological evaluations. Conclusions: Lutein co-administration was highly effective in prevention of cisplatin-induced retinal damage due to the anti-oxidant and anti-inflammatory effects of lutein.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2018Protective effects of rutin against methanol induced acute toxic optic neuropathy: An experimental study
Taşlı, Nurdan Gamze; Çimen, Ferda Keskin; Karakurt, Yücel; Uçak, Turgay; Mammadov, Renad; Süleyman, Bahadır; Kurt, Nezahat; Süleyman, Halis
AIM: To determine the effects of Rutin on methanol induced optic neuropathy and compare the results with the effects of ethanol. METHODS: Totally 30 rats were divided into 5 groups, with 6 rats in each group as follows: healthy controls (C), methotrexate (MTX), methotrexate+methanol (MTM), methotrexate+methanol+ethanol (MTME) and methotrexate+ methanol+Rutin (MTMR). In all rabbits except those of the control group, MTX, diluted in sterile serum physiologic, 0.3 mg/kg per oral was applied for 7d by the aid of a tube. After this procedure to the rats of MTM, MTME and MTMR groups, 20% methanol with a dose of 3 g/kg per oral was given by the aid of a tube. In MTME group, 4h after the application of methanol, 20% ethanol was applied by the same way with a dose of 0.5 g/kg. On the other hand, in MTMR group 4h after the application of methanol, Rutin, which was dissolved in distilled water, was applied by the same way with a dose of 50 mg/kg. RESULTS: There were statistically significant differences in tissue 8-hydroxy-2 deoxyguanine (8-OHdG), interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), myeloperoxidase (MPO). glutathione peroxidase (tGSH) and superoxide dismutase (SOD) levels between groups (P<0.001). In MTMR group tissue 8-OHdG, IL-1β, MDA, and MPO levels were similar with the healthy controls but significantly different than the other groups. In histopathological evaluations, in MTX group there was moderate focal destruction, hemorrhage and decrease in number of astrocytes and oligodendrocytes; in MTM group there was severe destruction and edema with decrease in number of astrocytes and oligodendrocytes; in MTME group there was mild hemorrhage, mild edema, mildly dilated blood vessels with congestion while in MTMR group, optic nerve tissue was resembling the healthy controls. CONCLUSION: Rutin may prevent methanol-induced optic neuropathy via anti-inflammatory effects and decreasing the oxidative stress. New treatment options are warranted in this disease to avoid loss of vision in patients.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2016The effect of anakinra on paclitaxel-induced peripheral neuropathic pain in rats
Kuyrukluyıldız, Ufuk; Küpeli, İlke; Bedir, Zehra; Özmen, Özgür; Onk, Didem; Süleyman, Bahadır; Mammadov, Renad; Süleyman, Halis
Objective: Paclitaxel is used in the treatment of cancer, and it may cause interleukin-1 beta (IL-1β)-related peripheral neuropathic pain. While our primary aim was to investigate the analgesic efficacy of an IL-1β antagonist, a secondary outcome was to assess whether a correlation exists between analgesic effects and antioxidant activity. Methods: A total of 24 albino Wistar male rats were divided into the following groups: paclitaxel-control, paclitaxel+50 mg kg−1 anakinra, paclitaxel+100 mg kg−1 anakinra and healthy group (HG). After the normal paw pain threshold in all animal groups was measured using a Basile algesimeter, a single dose of 2 mg kg−1 paclitaxel was intraperitoneally administered on the 1st, 3rd, 5th and 7th days. Anakinra was intraperitoneally administered following the final paclitaxel administration. The paw pain thresholds in the groups were measured before and seven days after paclitaxel administration and at the 1st and 3rd hours after anakinra administration. After the third hour of measurement, the rats were killed with high doses of ketamine, and the paw tissues were removed. Malondialdehyde, myeloperoxidase and total glutathione levels were measured in claw tissues, and IL-1β gene expression was determined. The biochemical results were compared with the results of the HG; in the meanwhile the claw pain threshold results were compared with the results obtained after the last paclitaxel and the results obtained from the 1st and 3rd hours after the anakinra application. Results: The claw paw pain threshold of the rats decreased one and three hours after anakinra administration. Further, 100 mg kg−1 anakinra had greater analgesic activity than 50 mg kg−1 anakinra. A correlation was found between the antioxidant and analgesic activities of 100 mg kg−1 anakinra. Conclusion: Anakinra may be useful to reduce paclitaxel-induced neuropathic pain; further, 100 mg kg−1 anakinra may have greater analgesic and antioxidant activities.
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